When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

DKA Management -Insulin Drip Protocol -RoundsRx

🔍 Overview

Definition

DKA is characterized by the triad of hyperglycemia (usually BG > 250 mg/dL), anion-gap metabolic acidosis (pH < 7.3, bicarb < 18), and ketonemia/ketonuria. It results from absolute or relative insulin deficiency combined with excess counterregulatory hormones.

Why It Matters

⚠ Mortality up to 5% in adultsHigher in elderly, delayed recognition, or severe comorbidities. Cerebral edema is the leading cause of death in children.

Who Gets It

Type 1 DM (can be the presenting illness in ~25%)
Type 2 DM under physiologic stress
SGLT2-inhibitor users (euglycemic DKA -BG may be < 200!)
Precipitants: infection (30–40% -most common), insulin omission/non-compliance (20–25%), new diagnosis T1DM, MI/ACS, pancreatitis, cocaine, alcohol

Mnemonic -5 I's of DKA Precipitants:
Infection (30–40%, #1 cause -UTI, pneumonia, skin) · Insulin (missed or inadequate doses) · Infarction (MI, stroke, mesenteric ischemia) · Intoxication (cocaine, alcohol, drugs) · Inflammation (pancreatitis, surgery, trauma)

Pathophysiology

Insulin deficiency → unrestrained lipolysis → free fatty acids → hepatic ketogenesis (acetoacetate, β-hydroxybutyrate) → high anion gap metabolic acidosis. Hyperglycemia → osmotic diuresis → profound volume depletion and electrolyte losses. Total body K⁺ is depleted even when serum K⁺ appears normal or high (due to transcellular shift from acidosis).

Presentation

Symptoms

Polyuria, polydipsia, nausea, vomiting, abdominal pain
Weakness, fatigue, altered mental status (in severe cases)
Timeline: hours to days (faster than HHS)

Exam

Kussmaul respirations (deep, rapid -compensating for acidosis)
Fruity/acetone breath
Signs of dehydration: dry mucosa, tachycardia, hypotension, poor skin turgor

Red Flags

Altered mental status → think cerebral edema, severe osmolarity
Potassium < 3.5 → do NOT start insulin until repleted
Euglycemic DKA (SGLT2i) -don't miss it
pH < 7.0 or bicarb < 10 → severe DKA, ICU threshold

Differential Diagnosis

HHS -BG often > 600, severe hypertonicity, no/minimal ketones, pH usually > 7.3
Alcoholic ketoacidosis -low or normal glucose, ketones present, history of binge drinking + poor PO
Starvation ketosis -mild, pH > 7.3, bicarb usually > 18
Other high AG acidosis -lactic acidosis, toxic ingestions (methanol, ethylene glycol, salicylates)

🧪 Workup & Diagnosis

Initial Workup

DO ALL OF THIS IMMEDIATELYThese tests diagnose DKA, guide fluid/insulin dosing, and identify precipitant -results change management NOW.

Labs (STAT)

BMP -BG, creatinine, K⁺, bicarbonate
VBG or ABG -pH, pCO₂, calculated bicarb
Anion gap = Na – (Cl + HCO₃) → normal 8–12; in DKA typically > 20
Beta-hydroxybutyrate (BHB), serum -≥ 3.0 mmol/L is diagnostic for DKA per ADA/EASD 2024. Preferred over urine ketones for both diagnosis AND monitoring resolution.
Urine ketones (only if serum BHB unavailable; moderate-to-large dipstick ketones is the fallback diagnostic threshold)
Phosphate, magnesium -often depleted
CBC, blood cultures -rule out infectious precipitant
Lipase -DKA can elevate lipase without true pancreatitis
HbA1c -assess chronic control
Urinalysis + urine culture
Pregnancy test (women of childbearing age)

Imaging / ECG

ECG -assess for hyperkalemia changes (peaked T waves, wide QRS) or ischemia as precipitant
CXR -rule out pneumonia as precipitant
CT head only if focal neuro deficits or concern for cerebral edema

Diagnostic Criteria for DKA UPDATED 2024

🔄 What changed in 2024 (ADA/EASD Consensus): Diagnosis now requires all three of the triad below, with BHB ≥ 3.0 mmol/L as the preferred ketone marker. Severity grading was simplified to pH and bicarb only, anion gap and mental status were removed (AG is confounded by hyperchloremic acidosis from NS; mental status is now used for ICU triage, not severity grading). Bicarb thresholds also shifted slightly.

Diagnostic Triad (all 3 required)

Hyperglycemia: glucose ≥ 200 mg/dL (or known diabetes; not required in euglycemic DKA on SGLT2i)
Ketosis: BHB ≥ 3.0 mmol/L (preferred) OR moderate-to-large urine ketones
Acidosis: venous pH < 7.3 OR serum bicarbonate < 18 mEq/L

Severity Grading (ADA/EASD 2024)

Parameter	Mild	Moderate	Severe	vs prior guideline
Venous pH	7.25–7.30	7.00–7.24	< 7.00	UNCHANGED
Bicarb (mEq/L)	15–18	10–<15	< 10	CHANGED mild now 15–18 (was 15–18, but resolution threshold raised)
Anion gap and mental status were removed from severity grading in 2024. AG is still elevated in DKA but is confounded by hyperchloremic acidosis after NS resuscitation. Altered mental status remains an independent ICU-triage criterion.

ADA/EASD Consensus, 2024

🚨 Management

Treatment: Step by Step

BEFORE STARTING INSULINEnsure K⁺ ≥ 3.5 mEq/L. Starting insulin with hypokalemia causes fatal cardiac arrhythmia.

First 5 Minutes

Assess & Stabilize
ABCs. IV access × 2. Foley if altered or unable to void. Cardiac monitor. POC glucose. Draw all STAT labs. Call senior if severe (pH < 7.1, AMS, K⁺ < 3.5).

First 15–30 Minutes

IV Fluids -Bolus Only If Hemodynamically Unstable
• Unstable / severely volume-depleted: 1-1.5 L isotonic crystalloid bolus over 1 hour (NS OR balanced).
• Stable: skip the bolus -start 250-500 mL/hr maintenance from the outset.
The reflex "2 L for everyone" is out; over-resuscitation is the more common modern error ADA DKA Consensus, 2024

After the first hour, choose by corrected Na⁺ (calculator):
• Corrected Na ≤ 135 → continue 0.9% NS at 250-500 mL/hr
• Corrected Na > 135 → switch to 0.45% NaCl at 250-500 mL/hr
• If using LR: just continue LR throughout and skip the half-NS switch (LR's Na 130 already provides some free water; only switch to 0.45% NaCl if corrected Na > 150).

Goal: replace 3-6 L deficit over 24-48 h (gentler is fine; over-aggressive correction risks cerebral edema, especially in pediatrics -PECARN, 2018).

🔄 Updated Practice: Old teaching was NS (normal saline) for DKA fluid resuscitation. Newer evidence (SMART, 2018) suggests balanced crystalloids (LR) may be preferred -NS causes hyperchloremic metabolic acidosis, which can worsen and confuse the clinical picture. The 4 mEq/L of potassium in LR is NOT a contraindication in hyperkalemic DKA -it's below physiologic plasma K⁺, and NS paradoxically worsens hyperkalemia via hyperchloremic acidosis (shifts K⁺ out of cells). Multiple trials show LR safely lowers serum K⁺ in DKA compared with NS.

First Hour

Potassium Replacement
K⁺ < 3.5 → replace aggressively (20–40 mEq/hr IV), do NOT start insulin yet
K⁺ 3.5–5.0 → add 20–30 mEq K⁺ per liter of IVF, start insulin
K⁺ > 5.0 → start insulin, hold K⁺ replacement, recheck in 2 hours

Insulin Infusion
Regular insulin drip at 0.14 units/kg/hr (no-bolus protocol, per ADA 2026). Alternative: 0.1 unit/kg IV bolus + 0.1 unit/kg/hr infusion. Target: BG drop of 50–75 mg/dL/hr.

🔄 Updated Practice: The old DKA protocol included an insulin IV bolus before starting the drip. Current ADA guidelines recommend NO bolus -start continuous infusion at 0.14 units/kg/hr directly. The bolus increased hypoglycemia risk without improving outcomes. Also: subcutaneous insulin protocols (insulin lispro/aspart q1-2h) are acceptable for mild-moderate DKA -IV is not always necessary.

When BG Hits 200–250 mg/dL

Switch to Dextrose-Containing Fluids
Add D5 to IV fluids (D5-0.45%NS) -reduce insulin drip to 0.05 units/kg/hr. Continue until anion gap closes, NOT just until BG normalizes. This is the most common resident mistake.

Resolution Criteria UPDATED 2024

Preferred (when BHB available):

Beta-hydroxybutyrate (BHB) < 0.6 mmol/L
AND patient tolerating PO / clinically improved

Alternative (BHB unavailable, ALL must be met):

Venous pH ≥ 7.3
Serum bicarbonate ≥ 18 mEq/L
Anion gap ≤ 10 mEq/L

ADA/EASD Consensus, 2024

🔄 What changed in 2024: BHB < 0.6 mmol/L is now the preferred resolution marker. Anion gap closure was a noisy endpoint, large-volume NS gives hyperchloremic acidosis, so the gap can stay wide even after ketones clear and patients get stuck on the drip. BHB measures the actual ketoacid driving DKA. Other changes: bicarb threshold raised from ≥ 15 to ≥ 18, anion gap tightened from ≤ 12 to ≤ 10, and glucose < 200 was dropped (you can resolve DKA while still hyperglycemic, and euglycemic DKA exists).

Transitioning to Subcutaneous Insulin

Give SQ long-acting insulin 2 hours before stopping the drip (overlap is mandatory to prevent rebound ketoacidosis) ADA/EASD Consensus, 2024. Resume home insulin regimen if known, or start TDD calculation (0.5–0.8 units/kg/day). Ensure patient is eating and K⁺ > 3.5.

When to Escalate to ICU

pH < 7.0 or bicarb < 10
Altered mental status / decreased GCS
Hemodynamic instability not responding to fluids
K⁺ < 3.0 or > 6.0 with ECG changes
Concurrent MI, stroke, or surgical emergency

Swipe for more examples

📋 Case 1, DKA Insulin Drip Management

Patient: 28F with T1DM, glucose 520, pH 7.15, bicarb 8, AG 28, K⁺ 5.8

Time	Action
Hour 0	Start insulin drip 0.14 units/kg/hr (no bolus). NS 1L/hr. Do NOT give K⁺ yet (K⁺ > 5.2).
Hour 2	Glucose 380 (↓140). K⁺ 4.5 → start KCl 20 mEq/hr in IV fluids. Continue insulin drip.
Hour 4	Glucose 280 (↓100/hr -on target). K⁺ 3.8 → increase KCl to 40 mEq/hr. AG closing (18).
Hour 6	Glucose 240 → approaching 250 threshold. Switch fluids to D5 1/2NS + KCl to prevent hypoglycemia while continuing insulin to close the gap.
Hour 8	Glucose 190, pH 7.32, bicarb 16, AG 12 (closing). K⁺ 4.0.
Hour 10	AG closed (AG 10), pH 7.38, bicarb 20, patient eating. → Overlap SC insulin (give long-acting + meal dose), wait 2 hours, THEN stop drip.

Key: Never stop insulin drip until: (1) BHB < 0.6 mmol/L (or if BHB unavailable, AG ≤ 10), (2) pH ≥ 7.3, (3) bicarb ≥ 18, (4) patient eating, AND (5) SC insulin given ≥ 2h prior.

📋 Case 2, Euglycemic DKA (SGLT2 Inhibitor)

Patient: 52F with T2DM on empagliflozin + metformin. Presents with nausea, vomiting, abdominal pain × 2 days. Glucose 185 (not elevated!). pH 7.18, bicarb 10, AG 24, ketones 5.2.

The trap: Glucose is near-normal → team almost missed DKA. SGLT2 inhibitors cause glycosuria → glucose stays low while ketoacidosis develops.

Treatment:

Stop empagliflozin immediately. Effects last 24–48h even after stopping.
Start D5NS + insulin drip, need dextrose from the start since glucose is already normal. Cannot let glucose drop further.
Aggressive K⁺ monitoring, same protocol as classic DKA.
Close the gap: Same endpoints, pH > 7.3, bicarb > 18, AG closed. Takes longer than classic DKA because you're limited by how fast you can run insulin with dextrose.

Key lesson: Always check a VBG/BMP on any patient on SGLT2i presenting with nausea/vomiting. Normal glucose does NOT rule out DKA. Check ketones and AG.

📋 Case 3, DKA with Severe Hypokalemia

Patient: 19M with T1DM, found unresponsive. Glucose 680, pH 6.95, bicarb 4, AG 36. K⁺ = 2.8.

Critical decision: K⁺ < 3.3 → DO NOT start insulin yet. Insulin drives K⁺ intracellular → can cause fatal arrhythmia.

Treatment:

Step 1: IV KCl 40 mEq/hr via central line (peripheral max 10 mEq/hr). Continuous telemetry. Recheck K⁺ every 1–2 hours.
Step 2: Aggressive IVF, NS 1L/hr. Fluids alone will lower glucose ~50–75 mg/dL/hr.
Step 3: Once K⁺ ≥ 3.3 → START insulin drip at 0.14 units/kg/hr. Continue K⁺ replacement aggressively.
Step 4: Consider bicarb ONLY if pH < 6.9 (give 100 mL of 8.4% NaHCO₃ in 400 mL sterile water over 2h). Controversial but ADA allows at pH < 6.9.

Key lesson: Always check K⁺ BEFORE starting insulin in DKA. K⁺ < 3.3 = replace first. This is the most dangerous moment in DKA management, insulin without adequate K⁺ kills.

💊 Medications & Doses

Medications & Dosing

Drug	Dose / Route	Indication	Key Points
Regular Insulin	0.14 units/kg/hr IV drip (no bolus) OR 0.1 units/kg/hr (with 0.1 units/kg IV bolus) ADA 2026	Insulin infusion	Do not start if K⁺ < 3.5. Reduce to 0.05 when BG < 250
Normal Saline (0.9%)	1–1.5 L over 1 hr, then 250–500 mL/hr	Volume resuscitation. LR is an acceptable alternative (SMART, 2018 -balanced crystalloids reduce AKI/death vs NS in critically ill)	Switch to 0.45%NS after initial bolus based on corrected Na⁺
KCl	20–40 mEq/hr IV (max 40 mEq/hr via central line) 10–20 mEq/hr peripheral	Hypokalemia in DKA	Continuous cardiac monitoring. Expect K⁺ to drop as insulin given
Sodium Bicarbonate	100 mEq in 400 mL D5W over 2 hrs	pH < 6.9 only	Controversial. May worsen hypokalemia and CNS acidosis. Use sparingly
Phosphate	20–30 mmol IV over 6 hrs	PO₄ < 1.0 mg/dL with symptoms	Routine replacement not recommended. Risk of hypocalcemia
Glargine (Lantus)	0.25–0.3 units/kg SQ (or prior home dose)	Transition off drip	Give 2 hours before stopping drip. Do not skip

📋 On Rounds

Common Pimp Questions

Why should you NOT start insulin if K⁺ < 3.5?

Insulin drives K⁺ intracellularly. Starting insulin when K⁺ is already low can cause life-threatening hypokalemia and fatal cardiac arrhythmia. Always replete first.

When do you stop the insulin drip?

Per ADA/EASD 2024: BHB < 0.6 mmol/L AND patient eating. If BHB unavailable, use the fallback triad: pH ≥ 7.3, bicarb ≥ 18, AG ≤ 10. NOT just when glucose normalizes. And give long-acting SQ insulin 2 hours before stopping the drip to prevent rebound ketosis.

What is euglycemic DKA and who is at risk?

DKA occurring with near-normal glucose (< 200 mg/dL). Seen with SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin). They enhance renal glucose excretion, masking hyperglycemia while ketoacidosis progresses. Always check ketones in SGLT2i users with nausea/vomiting.

Why is bicarbonate therapy generally avoided in DKA?

Bicarb worsens hypokalemia, may cause paradoxical CNS acidosis (CO₂ diffuses into CSF faster than bicarb), and has not been shown to improve outcomes. Reserve for pH < 6.9 only.

Clinical Examples

📋 Case 1, Classic DKA with Insulin Omission

Patient: 24 y/o F with T1DM, ran out of insulin 3 days ago, presents with nausea, vomiting, abdominal pain, and Kussmaul breathing.

Key findings: HR 118, BP 98/62, RR 28. BG 480, pH 7.12, bicarb 6, AG 28, K⁺ 5.4, BHB 6.8 mmol/L.

Management:

NS 1L bolus over 1h, then 0.45% NS at 250 mL/hr
K⁺ 5.4 (>3.5), start regular insulin drip at 0.14 units/kg/hr (no bolus), OR alternatively 0.1 u/kg IV bolus + 0.1 u/kg/hr drip ADA, 2026
Add KCl 20 mEq/L to each liter of IVF (total body K⁺ depleted despite normal serum K⁺)
When BG < 250, add D5 to IVF and reduce insulin to 0.05 units/kg/hr

Teaching point: Serum K⁺ is artificially elevated due to acidosis-driven transcellular shift. Total body K⁺ is always depleted in DKA. Aggressively replete as insulin drives K⁺ intracellularly.

📋 Case 2, Euglycemic DKA on SGLT2 Inhibitor

Patient: 58 y/o M with T2DM on empagliflozin and metformin, presents with 2 days of nausea, vomiting, and fatigue after a GI illness.

Key findings: BG 185, pH 7.22, bicarb 12, AG 22, BHB 5.2 mmol/L. K⁺ 4.1.

Management:

Recognize euglycemic DKA, glucose near-normal but AG acidosis with ketones
Hold SGLT2 inhibitor immediately
Start insulin drip + D10 infusion (glucose already low, needs dextrose from the start)
Volume resuscitate aggressively, SGLT2i causes osmotic diuresis

Teaching point: SGLT2 inhibitors mask hyperglycemia by enhancing renal glucose excretion. Always check ketones in SGLT2i users presenting with nausea/vomiting, even if glucose is normal.

📋 Case 3, DKA with Severe Hypokalemia

Patient: 31 y/o F with T1DM, presenting with DKA triggered by UTI. Found altered in the ED.

Key findings: BG 520, pH 7.08, bicarb 5, AG 30, K⁺ 2.9, ECG shows U waves and prolonged QTc.

Management:

DO NOT start insulin, K⁺ < 3.5 is an absolute contraindication
Aggressive K⁺ repletion: KCl 40 mEq/hr IV via central line with continuous telemetry
Start insulin ONLY when K⁺ ≥ 3.5 (recheck q1h during repletion)
Treat UTI precipitant with appropriate antibiotics

Teaching point: Insulin before K⁺ repletion in hypokalemic DKA causes fatal arrhythmias. This is the single most important safety rule in DKA management.

What to Say on Rounds

📋 Sample Presentation

"Mr. Smith is a 32-year-old with Type 1 DM presenting with a 2-day history of nausea, vomiting, and abdominal pain in the setting of missed insulin doses. He was found to have a glucose of 420, pH 7.18, bicarb of 10, and an anion gap of 24, consistent with severe DKA. He was started on NS resuscitation and a regular insulin drip at 0.1 units/kg/hr after K⁺ was confirmed to be 3.8. Over the past 8 hours, his glucose has come down to 240, his anion gap has narrowed to 14, and his bicarb is now 16. We are targeting gap closure before transitioning to subcutaneous insulin. His precipitant appears to be medication non-adherence, and we are involving diabetes education."

Monitoring Schedule

During Active DKA

Glucose: every 1 hour (via POC meter)
BMP (or at least K⁺, bicarb): every 2–4 hours
Anion gap: calculated every 2–4 hours to confirm closure
Beta-hydroxybutyrate: every 4 hours (preferred over urine ketones)
Urine output: target ≥ 0.5 mL/kg/hr -place Foley if needed
ECG: if K⁺ < 3.0 or > 6.0

Pitfalls to Watch

Stopping insulin too early -always wait for AG closure, not just BG normalization
Forgetting the 2-hour overlap when transitioning to SQ insulin
Overcorrecting fluids -iatrogenic fluid overload, especially in elderly or cardiac patients
Missing the precipitant -always ask: why did they get DKA?
Euglycemic DKA on SGLT2i -BG may be near-normal; check ketones regardless
Cerebral edema -rare in adults but watch for headache, declining GCS during treatment

Complications

Hypokalemia (from insulin shifting K⁺ intracellular)
Hypoglycemia (from excess insulin or failure to add dextrose)
Cerebral edema (especially children, rapid fluid shifts)
ARDS (from aggressive fluid resuscitation)
Thrombosis (hypercoagulable state)

Before Discharge

Patient tolerating PO fluids and meals
On appropriate SQ insulin regimen
BG < 200, AG closed, K⁺ repleted
Precipitant identified and addressed
Diabetes education arranged
Endocrine follow-up within 1–2 weeks

⚡ Summary

One-Screen Summary

Definition

BG > 250 + pH < 7.3 + bicarb < 18 + anion gap > 10 + ketones. Triad must all be present.

Precipitants

Infection (30–40%), missed insulin (20–25%), new DM, MI, pancreatitis, SGLT2i use

Initial Management

IV NS 1L bolus → check K⁺ → if K⁺ ≥ 3.5 start regular insulin 0.1 u/kg/hr → replace K⁺ in IVF

Key Rule

Add D5 when BG < 250. Stop drip only when AG closed. Overlap SQ insulin 2 hrs before stopping drip.

Biggest Pitfalls

Starting insulin with K⁺ < 3.5. Stopping insulin when BG normalizes (not when AG closes). Missing euglycemic DKA on SGLT2i.

ICU Threshold

pH < 7.0, bicarb < 10, AMS, hemodynamic instability, K⁺ < 3.0 with ECG changes

📄 One Pager

ICU / Endocrine · One Pager

Diabetic Ketoacidosis

Hyperglycemia + anion-gap acidosis + ketones. Fluids first. Check K⁺ before insulin. Close the gap, not just the glucose.

🧪 Diagnosis

BG > 250 mg/dL
pH < 7.3 / Bicarb < 18
Anion gap > 10–12
Ketones positive (serum BHB preferred)
Euglycemic DKA: BG normal on SGLT2i

⚡ Precipitants

Infection (30–40%)
Missed insulin (20–25%)
New diagnosis T1DM
MI, pancreatitis, surgery
SGLT2 inhibitor use

🚨 Management -Step by Step

1

IV fluids: 1–1.5L NS over 1h → then 0.45%NS at 250–500 mL/hr

2

Check K⁺ BEFORE insulin -if < 3.5, replace first. Do NOT start insulin.

3

Insulin: Regular insulin 0.14 units/kg/hr IV (no bolus), OR 0.1 u/kg IV bolus + 0.1 u/kg/hr drip ADA 2026

4

When BG < 250: Add D5 to IVF, reduce insulin to 0.05 units/kg/hr

5

Stop drip when: BG < 200 + AG ≤ 12 + bicarb ≥ 15 -NOT just BG normal

6

SQ insulin overlap: Give long-acting 2h before stopping drip

💊 Key Drugs

Regular insulin0.1 u/kg/hr

KCl20–40 mEq/hr IV

NS → 0.45%NS250–500 mL/hr

Glargine0.25 u/kg SQ

📊 Monitoring

BG every 1h (POC)
BMP q2–4h
Anion gap q2–4h
BHB q4h
UOP ≥ 0.5 mL/kg/hr

⚠️ Pitfalls

Insulin with K⁺ < 3.5
Stopping drip at BG normal
Missing euglycemic DKA
No SQ overlap
Missing precipitant

🏥 ICU Threshold

pH < 7.0 / bicarb < 10
Altered mental status
Hemodynamic instability
K⁺ < 3.0 with ECG changes

🎓 Key Trial

ADA 2026: No IV insulin bolus -drip only at 0.1 u/kg/hr
Resolution: Gap closure, not glucose normalisation
Bicarb: Only if pH < 6.9 (not routine)

Diabetic Ketoacidosis (DKA)